title: Assessment of dental fluorosis in Mmp20 +/- mice.
abstract: The molecular mechanisms that underlie dental fluorosis are poorly understood. The retention of enamel proteins hallmarking fluorotic enamel may result from impaired hydrolysis and/or removal of enamel proteins. Previous studies have suggested that partial inhibition of Mmp20 expression is involved in the etiology of dental fluorosis. Here we ask if mice expressing only one functional Mmp20 allele are more susceptible to fluorosis. We demonstrate that Mmp20 (+/-) mice express approximately half the amount of MMP20 as do wild-type mice. The Mmp20 heterozygous mice have normal-appearing enamel, with Vickers microhardness values similar to those of wild-type control enamel. Therefore, reduced MMP20 expression is not solely responsible for dental fluorosis. With 50-ppm-fluoride (F(-)) treatment ad libitum, the Mmp20 (+/-) mice had F(-) tissue levels similar to those of Mmp20 (+/+) mice. No significant difference in enamel hardness was observed between the F(-)-treated heterozygous and wild-type mice. Interestingly, we did find a small but significant difference in quantitative fluorescence between these two groups, which may be attributable to slightly higher protein content in the Mmp20 (+/-) mouse enamel. We conclude that MMP20 plays a nominal role in dental enamel fluorosis.
authors.affiliation: Department of Cytokine Biology, The Forsyth Institute, Harvard School of Dental Medicine, Boston, MA 02115, USA.
authors.forename: R
authors.initials: R
authors.lastname: Sharma
authors.forename: C E
authors.initials: CE
authors.lastname: Tye
authors.forename: A
authors.initials: A
authors.lastname: Arun
authors.forename: D
authors.initials: D
authors.lastname: MacDonald
authors.forename: A
authors.initials: A
authors.lastname: Chatterjee
authors.forename: T
authors.initials: T
authors.lastname: Abrazinski
authors.forename: E T
authors.initials: ET
authors.lastname: Everett
authors.forename: G M
authors.initials: GM
authors.lastname: Whitford
authors.forename: J D
authors.initials: JD
authors.lastname: Bartlett
mesh_terms: D000566:Amelogenesis; D000818:Animals; D003743:Dental Enamel / Q000737:chemistry / Q000201:enzymology; D003746:Dental Enamel Proteins / Q000378:metabolism; D004658:Enamel Organ / Q000201:enzymology; D005453:Fluorescence; D005459:Fluorides / Q000009:adverse effects*; D009050:Fluorosis, Dental / Q000201:enzymology* / Q000209:etiology* / Q000235:genetics; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects*; D006244:Hardness; D006579:Heterozygote; D006720:Homozygote; D053519:Matrix Metalloproteinase 20 / Q000032:analysis / Q000096:biosynthesis* / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL
chemical_list: D003746:Dental Enamel Proteins; D053519:Matrix Metalloproteinase 20; D005459:Fluorides